Canine eczema, clinically known as dermatitis rubric madidans, is one of the most difficult dermatologic problems to treat in veterinary medicine. Its pathogenesis is still rudimentary and multiple therapies are available to treat symptoms, while antibiotics quell secondary infections. Older literature refers to this entity as a moist and desquamating eczema or as infectious dermatitis, as the etiology was theorized to be Staphylococcus aureus as the putative pathogen. This Staph was cultured from early lesions, thus the term "infectious dermatitis." Staph toxins or an "allergic id" reaction were postulated as etiologic. Contact dermatitis might also play a role in this condition.
Clinically, this eczema presents an acute discomfort, is persistent, and tends to recur. It is more frequent in the mature dog rather than in puppies. The lesions are of sudden onset and spread rapidly. The affected areas are very sensitive and extremely pruritic. The animal may have premonitory symptoms which include restlessness, anorexia, vomiting, and itching. Animals tend to persist in scratching, biting and rubbing the affected sensitive, moist lesions which become yellow to light red in color. Their efforts to obtain relief of the pruritus by scratching not only extends the depth and surface area of the dermatitis, but the excriations cause infection which extend to areas adjoining the original eczematoid site. Fever and lymph node enlargement may be noted. The course of this eczematoid reaction is variable, depending on the extent of the lesion, degree of destruction of the cutaneous tissues, severity of secondary infection and the animal's response to therapy.
Infections of the skin, so-called integumentary infections in dogs and cats, are most frequently caused by bacterial or fungal infectious agents. The cutaneous microbial flora comprises both resident and transient bacterial inhabitants. The former tends to be consistent in types and colonies within an anatomic area and is usually harmless. Resident bacteria have the usual characteristic of inhibiting the growth of skin pathogenic bacteria.
Other factors maintaining the resident communal micro-flora include skin pH and moisture, sebum production and the healthy status of the outer skin layer, the stratum corneum. Under adverse conditions to the aforementioned cutaneous factors which may disrupt the normal bacterial barriers, both the resident (usual) bacteria and the transient bacterial invaders may cause the cutaneous infectious lesion called pyoderma. In dogs, Staphylococcus aureus is a normal skin inhabitant but may increase its colony numbers in traumatized, inflamed or seborrheic animal skin conditions. Staph may reside in the hair, and these bacteria are apt to be the source of secondary infection causing pyoderma, with the classic symptoms of the animals' "hot spots".
While Staph aereus is the major pathogen isolated from dogs' pyoderma, both local and systemic immune responses are probably involved in the pathogenesis of pyoderma. While specific anti-microbials are mandatory for the eradication of the pathogen causing pyoderma, both symptomatic and anti-inflammatory therapy to these cutaneous lesions is mandatory. The synergistic antioxidant compositions of the present invention are designed to scavenge and neutralize the reactive oxygen and other free radical species, which are present in the inflammatory reactions of these cutaneous primary and secondary infections and inflammatory reactions. Pustules, papules and furuncles require specific anti-microbial therapies, plus symptomatic therapies, including the reduction of inflammatory free radical reactions by the present antioxidant synergistic components to enhance the animal's cutaneous endogenous antioxidant defenses and promote the healing reparative processes.
Secondary skin lesions, the pyodermas, are characterized by excoriations, and ulcerations and crusting. Excoriations are self-inflicted lesious leading to ulcers, which are commonly referred to as "hot spots". These "hot spots" are not truly pyoderma but are very bothersome and symptomatic to these domestic animals. Erosions and ulcers are secondary lesions, which result from the putative inflammatory process and/or from the victim's self-mutilation symptomatic response to the itching and pain. These are followed by classic signs of infection, namely, exudation, swelling and exaggerated redness and pus. The eroded and ulcerated tissues must be treated to alleviate the symptoms, and to reduce the inflammation. These remedies include compositions such as topicals containing the synergistic antioxidant complex of the present invention. Scarring needs to be prevented. Finally, if untreated, these secondary lesions, called "crusts" developing from dried exudates and keratin, must be carefully removed by the clinician in an effort to promote healing and avoid scarring of these tissues.
Infestation by fleas is common in domestic animals, particularly in dogs and cats, but fleas are not uncommon in other hairy mammals. Fleas are small, wingless bloodsucking external parasites, mainly of the species Ctenocephalides, genus felis for cats and genus canis for dogs. The adult flea spends most of its life on the body of the host. Eggs laid on the host or in the ground hatch into larvae feeding on organic matter. The larvae then spins a loose cocoon that within six days, under optimum conditions, becomes an adult then the insect emerges from the cocoon, and seeks the appropriate host, like these domestic animals, in order to feed on them and thereby continue their insect life cycle.
Adult fleas feed only on blood of the host animal. In this "nutrition and survival cycle"0 of the fleas, they cause their hosts intense itching (pruritus) with consequent irritation to the host, which evokes a response to scratch and bite the affected irritated skin in an effort to control the pruritic and inflammatory site of the hypersensitive host skin.
The fleas cause the irritating symptoms due to their constant biting of the host's skin and from the flea's salivary secretion of toxic agents and allergens. Particularly in hypersensitive domestic host animals, fleabites produce intense pruritus and the animal then scratches and bites the putative skin surfaces. These mammals become restless from the cutaneous irritation and they continue biting and scratching in an attempt to relieve the irritating symptoms. By this mechanism, the host produces an acute, discrete dermatitis, which has also commonly been called a "hot spot". Also, the biting and scratching may yield a chronic, nonspecific dermatitis, including ulceration and moist desquamation from the flea infested sites. The "hot spots" in the dog are usually subauricular, interscapular or adjacent to their rumps or thighs. In contrast, the chronic, non-specific flea induced dermatitis is more apt to be restricted to the lower back and to the perineum. Secondary infection from skin bacteria is common in both syndromes and may follow from the self-inflicted trauma of the host to a cycle of constant irritation, pruritus, ulceration and desquamation of the affected skin areas.
Diagnosis of these flea induced "hot spots" depends on careful examination of the "hot spots" and adjacent tissues for fleas or debris of fleas in the hair follicles. Fleas may also be found in large numbers in the head, rump or tail of the affected domestic animal.
Treatment is bi-modal and requires both symptomatic and specific therapy of the inflamed, ulcerated, and desquamated cutaneous lesions as well as eradication of the pathogen, the offending fleas. Insecticides may remove fleas from the host (pyrethrum or rotenone powders). Control of flea breeding places is environmentally imperative.
Treatment of the host is directed at controlling symptoms of itching and discomfort, to alleviate the animal's biting and scratching. The second line of therapy of "hot spots" is directed to reduce the inflammation and the toxic free radical species generated in this inflammatory reaction. One of the roles of this invention is in providing antioxidants which by scavenging and neutralizing free radicals in "hot spots," inflammation is reduced. By applying the present group of antioxidants based on L-glutathione and its synergistic antioxidant compositions, one is able to combat the skin's free radicals and the fleas' other toxic secretions and thereby heal "hot spots".
The antioxidant compositions of this invention may include as optional ingredients antimicrobials including antibiotics to help combat the secondary bacterial infections of these cutaneous, flea created "hot spots". These compositions may also contain the specific flea killing insecticides, as well as compounds known to provide anti-pruritic and soothing cutaneous effects to the animals' "hot spots". In summary, the compositions of this invention are based on antioxidants to ameliorate the inflammatory reaction and can optionally include as topical preparations compounds to provide both symptomatic and antimicrobial therapeutic effects such as bacitracin, neomycin, and/or polysporin. Oral or parenteral agents with anti-inflammatories can also be included such as cortisone, prednisolone, and aspirin or non-steroidal anti-inflammaries, plus optionally, tranquilizers and phenobarbital derivatives. Vital adjuncts in the management of "hot spots" include cleansing of the dermatitic, ulcerated areas with standard soaps and anti-microbial lotions, ideally with hexachlorophene. The mainstay to reduce inflammation and promote healing of "hot spots" is the use of the present antioxidant complex with eradication of the fleas.
Domestic animals not infrequently become infected with mites, which may cause pronounced itching with swelling and irritation of their skin. The itching may be severe necessitating the animal to scratch causing the skin to ulcerate. Symptoms are worse in warm weather. Secondary skin infections are serious complications. The intense scratching also spreads the mite, aggravating this condition which is known as sarcoptic mange. To establish the diagnosis, the causative mite needs to be identified and then eradicated by specific pesticide therapy. The animal's mite induced dermatitis and ulcerations require symptomatic treatment; the synergistic antioxidant compositions of this invention are used to reduce the redness and swelling of the inflammatory reaction while the zinc moieties help heal these sarcoptic mange lesions.
Another related condition which may also be treated with these antioxidant complexes to reduce redness, swelling and itching is called demodectic or red mange. This is caused by a small and elongated mite called Demodex folliculorum, which lives deep in the hair follicles, thereby becoming a more permanent invading parasite. Red mange in the dog usually starts in the head, around the eyes and then spreads producing a severe dermatitis with inflammation, thus the name red mange. Treatment again is directed at eliminating the mite, such as with Ivermectin, and along with the symptomatic therapy as the antioxidant compositions of this invention to reduce the inflammation, redness and itching. Oral Ivermectin has also been used for therapy of generalized demodicosis or scabies with good results.